Hormone Receptor Status in Breast Cancer

Why estrogen and progesterone receptor tests are important

In This Article

Hormone receptor status is an important aspect of breast cancer treatment. Determining your tumor's status is a high priority after a breast biopsy or breast-cancer surgery (mastectomy or lumpectomy). Whether you're positive (meaning estrogen and/or progesterone drives the growth of cancer cells) or negative (meaning one does not) will have a big impact on the next steps you take.

hormone receptor status in breast cancer
Verywell / Gary Ferster

Hormone Receptors & Receptor Tests

All breast cancers are examined under a microscope for biomarkers of estrogen and progesterone receptors. About 70% of breast cancers are hormone receptor-positive.

Your hormone receptor status should appear on your pathology report after biopsy or surgery. Receptors will be retested if you ever have a recurrence or metastases as well, as your status can change.

Hormones and receptors go together kind of like a lock and key. Receptors are proteins on the surface of breast cells, and when hormones bind to them, the receptors tell the cells to grow and divide. All breast cells have receptors, but they are found in much greater numbers on breast cancer cells that are considered positive.

A goal of treatment is to block the signal created when the hormones attach to receptors. Doing that requires one of two things:

  1. Reducing the amount of the hormone in the body
  2. Blocking the receptor so that hormone can't bind with it

Most of the time, breast cancers tend to be positive or negative for both estrogen and progesterone receptors. Now and then, one will be positive for estrogen but not progesterone. The treatment is the same either way.

Hormone Receptor Status Scores

Your hormone status scores should be on your pathology report. They're expressed as a number between 0 and 3.

Score Meaning
0 No receptors found
1+ Small number of receptors found
2+ Medium number of receptors found
3+ Large number of receptors found

Your report may also include the percentage of cells that tested positive for hormone receptors. Zero percent means no receptors were found and 100 percent means all the tested cells had receptors.

Why Your Hormone Status Matters

Breast cancers that are estrogen receptor-positive (ER+) and/or progesterone receptor-positive (PR+) are "fueled" by hormones. They're different from breast cancers that are HER2-positive, in which tumor growth is driven by growth factors that bind to HER2 receptors on the cancer cells. Breast cancers that don't have any of these receptors are called triple-negative.

Some breast cancers are both hormone receptor-positive and HER2-positive, meaning that estrogen, progesterone, and growth factors can stimulate cell growth. These cancers are often referred to as triple-positive breast cancers.

An ER+ or PR+ score means that hormones are causing your tumor to grow and hormone suppression treatments are likely to work well.
If the score is negative (ER- or PR-), then your tumor is not driven by hormones and your results will need to be evaluated along with other tests, such as your HER2 status, to determine the most effective treatment.

If the only information you're given is that your hormone status tests are negative, it's good to ask your doctor for a number that indicates the actual score. Even if the number is a low one, the tumor may effectively be treated with hormone therapy.

Treatment Options

If your tumor is ER+ and/or PG+, hormonal therapy is usually recommended. The choice of medications, however, depends on your menopausal status.

Before menopause, the ovaries produce the greatest amount of estrogen. To prevent this estrogen from fueling your cancer cells, medications called selective estrogen receptor modulators are used. These drugs, such as tamoxifen, bind to the estrogen receptor so that estrogen can't get to it.

After menopause, the situation is different because you have a lot less estrogen in the body. The primary source of post-menopausal estrogen is your body's conversion of androgens (male-type hormones) into estrogen. This reaction is catalyzed by an enzyme known as aromatase. Medications called aromatase inhibitors can block this enzyme so your body can't produce estrogen, thus starving the tumor.

Three aromatase inhibitors are available:

These drugs may sometimes be used in pre-menopausal women after ovarian suppression therapy. After first taking medications that prevent the ovaries from making estrogen or, in some cases, have their ovaries removed, these women are switched from tamoxifen to an aromatase inhibitor. This strategy appears to give some a better survival advantage.

Bisphosphonates can be used along with aromatase inhibitors for early-stage post-menopausal ER+ breast cancers as well. This appears to reduce the risk of recurrence and especially the spread of breast cancer to the bones.

With early-stage breast cancer that is estrogen receptor-positive, hormonal therapies can reduce the risk of recurrence by roughly half.

Other hormonal therapies may be used at times, too. A drug called Faslodex (fulvestrant) is a selective estrogen receptor down-regulator (SERD). It's sometimes used to treat women whose cancer progresses while they're on tamoxifen or an aromatase inhibitor. In addition, other hormonal therapies for metastatic breast cancer may be considered for some people.

Length of Treatment

In the past, treatment with tamoxifen or aromatase inhibitors was usually continued for five years. Studies have shown, though, that in women with a high risk of recurrence, longer treatment can be beneficial. It's important to talk to your doctor about current recommendations for length of treatment in light of these new studies.

Was this page helpful?

Article Sources

Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial policy to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
  1. Lumachi F, Brunello A, Maruzzo M, Basso U, Basso SM. Treatment of estrogen receptor-positive breast cancer. Curr Med Chem. 2013;20(5):596-604.

  2. Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. Signaling Molecules and Their Receptors.Available from: https://www.ncbi.nlm.nih.gov/books/NBK9924/

  3. Masoud V, Pagès G. Targeted therapies in breast cancer: New challenges to fight against resistanceWorld J Clin Oncol. 2017;8(2):120–134. doi:10.5306/wjco.v8.i2.120

  4. Badowska-Kozakiewicz AM, Patera J, Sobol M, Przybylski J. The role of oestrogen and progesterone receptors in breast cancer - immunohistochemical evaluation of oestrogen and progesterone receptor expression in invasive breast cancer in womenContemp Oncol (Pozn). 2015;19(3):220–225. doi:10.5114/wo.2015.51826

  5. Kurosumi M. Immunohistochemical assessment of hormone receptor status using a new scoring system (J-Score) in breast cancer. Breast Cancer. 2007;14(2):189-93.

  6. Prabhu JS, Korlimarla A, Desai K, et al. A Majority of Low (1-10%) ER Positive Breast Cancers Behave Like Hormone Receptor Negative TumorsJ Cancer. 2014;5(2):156–165. Published 2014 Jan 23. doi:10.7150/jca.7668

  7. Callahan R, Hurvitz S. Human epidermal growth factor receptor-2-positive breast cancer: Current management of early, advanced, and recurrent diseaseCurr Opin Obstet Gynecol. 2011;23(1):37–43.

  8. Aysola K, Desai A, Welch C, et al. Triple Negative Breast Cancer - An OverviewHereditary Genet. 2013;2013(Suppl 2):001. doi:10.4172/2161-1041.S2-001

  9. You SH, Chae BJ, Eom YH, et al. Clinical Differences in Triple-Positive Operable Breast Cancer Subtypes in Korean Patients: An Analysis of Korean Breast Cancer Registry DataJ Breast Cancer. 2018;21(4):415–424. doi:10.4048/jbc.2018.21.e53

  10. Fan W, Chang J, Fu P. Endocrine therapy resistance in breast cancer: current status, possible mechanisms and overcoming strategiesFuture Med Chem. 2015;7(12):1511–1519. doi:10.4155/fmc.15.93

  11. Jordan VC. The role of tamoxifen in the treatment and prevention of breast cancer. Curr Probl Cancer. 1992;16(3):129-76.

  12. Majumder A, Singh M, Tyagi SC. Post-menopausal breast cancer: from estrogen to androgen receptorOncotarget. 2017;8(60):102739–102758. Published 2017 Oct 27. doi:10.18632/oncotarget.22156

  13. Schneider R, Barakat A, Pippen J, Osborne C. Aromatase inhibitors in the treatment of breast cancer in post-menopausal female patients: an updateBreast Cancer (Dove Med Press). 2011;3:113–125. Published 2011 Oct 4. doi:10.2147/BCTT.S22905

  14. Fabian CJ. The what, why and how of aromatase inhibitors: hormonal agents for treatment and prevention of breast cancerInt J Clin Pract. 2007;61(12):2051–2063. doi:10.1111/j.1742-1241.2007.01587.x

  15. Blackburn SA, Parks RM, Cheung KL. Fulvestrant for the treatment of advanced breast cancer. Expert Rev Anticancer Ther. 2018;18(7):619-628.

  16. van Hellemond IEG, Geurts SME, Tjan-Heijnen VCG. Current Status of Extended Adjuvant Endocrine Therapy in Early Stage Breast CancerCurr Treat Options Oncol. 2018;19(5):26. Published 2018 Apr 27. doi:10.1007/s11864-018-0541-1

Additional Reading